Oxidative stress in the liver and the brain of rats in fulminant hepatic failure.

Abstract

The etiological mechanisms of brain edema in fulminant hepatic failure are incompletely understood. In a surgical model of fulminant hepatic failure in the rat, we tested whether oxidative stress may be involved in the early steps of brain edema. Moreover, we took advantage of this model to determine if oxidative stress may be involved in the hepatocyte dysfunction observed in the setting of fulminant hepatic failure. Oxidative stress was evaluated by measurement of tissue ascorbic acid in the brain and liver of rats at 6 hours after induction of fulminant hepatic failure versus in control or partially hepatectomized rats. After 6 hours, the level of ascorbic acid was not different in the brain tissue of the various groups, indicating no oxidative stress. The liver showed a significant decrease in ascorbic acid levels, both in ischemic and nonischemic liver tissue, suggesting that oxidative stress might be involved in the failure of liver regeneration in fulminant hepatic failure. In this rat model no oxidative stress was demonstrated in the brain during the early phase of fulminant liver failure.